Skip to main content
. Author manuscript; available in PMC: 2013 Jan 14.
Published in final edited form as: Nat Rev Gastroenterol Hepatol. 2012 Feb 7;9(4):199–208. doi: 10.1038/nrgastro.2012.9

Figure 3.

Figure 3

Loss of ATRX or DAXX function in pancreatic neuroendocrine tumors (PanNETs) correlates with the alternative lengthening of telomeres (ALT) phenotype. a | Immunolabeling for ATRX demonstrates strong nuclear labeling of ATRX protein in a well-differentiated PanNET. b | Immunolabeling for DAXX of the same PanNET demonstrates strong nuclear labeling of tumor nuclei. c | The same PanNET is negative for the ALT phenotype. Telomere florescence in situ hybridization (FISH) signals (red) are markedly dimmer in neoplastic cells (asterisk) than in the surrounding stromal cells. Centromere-specific FISH probe (green) serves as a positive control for hybridization. d | ATRX immunolabeling in a PanNET with ATRX mutation showing loss of nuclear protein expression. e | Telomere-specific FISH of the same PanNET displaying large, ultrabright telomere FISH signals indicative of ALT (white arrows). All images 400× original magnification.